It is a big challenge to achieve pure-blue (≤470 nm) perovskite light-emitting diodes (PeLEDs) with high efficiency and stability. Here, we report pure-blue (electroluminescence at 469 nm) PeLEDs with a full width at halfmaximum of 21 nm, high external quantum efficiency of 10.3%, luminance of 12 060 cd m −2 , and continuous operation half-life of 25 h, representing the stateof-the-art performance. This design is based on strongly quantum confined CsPbBr 3 quantum dots (QDs) with suppression of Auger recombination, which was enabled by inorganic ligands, replacing initial organic ligands on the QDs. The inorganic ligand acts as a "capacitor" to alleviate the charge accumulation and reduce the exciton binding energy of the QDs, which suppresses the Auger recombination, resulting in much lower efficiency roll-off of PeLEDs. Thus, the devices maintain high efficiency (>10%) at high luminance (>2000 cd m −2 ), which is of considerable significance for the display application.
Perovskite colloidal quantum wells (QWs) are promising to realize narrow deep-blue emission, but the poor optical performance and stability suppress their practical application. Here, we creatively propose a water-driven synthesis strategy to obtain size-homogenized and strongly confined deep-blue CsPbBr 3 QWs, corresponding to three monolayers, which emit at the deep-blue wavelength of 456 nm. The water controls the orientation and distribution of the ligands on the surface of the nanocrystals, thus inducing orientated growth through the Ostwald ripening process by phagocytizing unstable nanocrystals to form well-crystallized QWs. These QWs present remarkable stability and high photoluminescence quantum yield of 94 %. Furthermore, we have prepared light-emitting diodes based on the QWs via the all-solution fabrication strategy, achieving an external quantum efficiency of 1 % and luminance of 2946 cd m À 2 , demonstrating state-of-the-art brightness for perovskite QW-based LEDs.
Oxidative stress is an important pathogenic manifestation of Alzheimer's disease (AD) that contributes to synaptic dysfunction, which precedes Aβ accumulation and neurofibrillary tangle formation. However, the molecular machineries that govern the decline of antioxidative defence in AD remains to be elucidated, and effective candidate for AD treatment is limited. Here, we showed that the decreases in the inhibitor of apoptosis-stimulating protein of p53 (iASPP) was associated with the vulnerability to oxidative stress in the amyloid precursor protein (APP)/presenilin 1 (PS1) mouse brain. Treatment with an antioxidant, syringin, could ameliorate AD-related pathologic and behavioural impairments. Interestingly, syringin treatment resulted in an upregulation of iASPP and the increase in the interaction of iASPP with Kelchlike ECH-associating protein 1 (Keap1). Syringin reduced neuronal apoptosis independently of p53. We confirmed that syringin-induced enhancement of antioxidant defenses involved the stabilization of Nrf2 in overexpressing human Swedish mutant APP (APPswe) cells
in vitro
. Syringin-mediated Nrf2 nuclear translocation facilitated the activation of the Nrf2 downstream genes
via
iASPP/Nrf2 axis. Our results demonstrate that syringin-mediated increases of iASPP-Keap1 interaction restore cellular redox balance. Further study on the syringin-iASPP interactions may help in understanding the regulatory mechanism and designing novel potent modulators for AD treatment.
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